白杨素对哮喘模型小鼠肺组织核因子-κB表达的影响

Effects of chrysin on the expression of nuclear factor-κB in a murine model of asthma

目的 :观察白杨素对急性哮喘模型小鼠肺组织核因子(nuclear factor,NF)-κB表达的影响。方法 :24只雌性BALB/c小鼠随机分成4组:正常对照组、哮喘组、白杨素组、布地奈德组,每组6只。使用卵白蛋白腹腔注射致敏,气道激发制备哮喘模型,白杨素组小鼠给予白杨素50 mg/kg灌胃,布地奈德组小鼠给予布地奈德雾化液雾化吸入。肺功能测定评价小鼠气道阻力,HE染色评价小鼠气道炎症,酶联免疫吸附(ELISA)法检测支气管肺泡灌洗液(BALF)中白介素(IL)-4、IL-13和血清总Ig E的水平,Western blot检测肺组织NF-κB蛋白表达。结果 :哮喘组小鼠气道炎症和气道高反应性明显加重,白杨素能够显著抑制哮喘模型小鼠的气道炎症和气道高反应性,白杨素能够抑制哮喘小鼠BALF中IL-4、IL-13和血清总Ig E水平。哮喘组小鼠肺组织高表达的NF-κB水平,经白杨素治疗后显著降低。结论:白杨素能够抑制哮喘小鼠的气道炎症和气道高反应性,其机制可能与抑制肺组织NF-κB的表达有关。

Objective：To observe the effects of chrysin on the expression of nuclear factor （NF）-κB in lung tissues in a murine model of asthma. Methods： Twenty-four female BALB/c mice were randomly divided into 4 groups, including control group, asthma group, chrysin group and budesonide group. BALB/c mice were sensitized by intraperitoneal injection and challenged via the airway with ovalbumin （OVA）. Mice in the chrysin group were intragastrically administered with chrysin （50 mg/kg）. Mice in the budesonide group were exposed to aerosolized budesonide. Pulmonary functions were measured to evaluate the resistance of expiration. The sections were stained with either hematoxylin ＆ eosin to assess the inflammatory cell infihrates. The levels of interleukin IL-4 and IL-13 in bronchoalveolar lavage fluid （BALF） and total immunoglobuhn E （IgE） levels in serum were measured by ELISA. The protein expression of NF-κB in lung tissues was determined by Western blotting assay. Results： Airway inflammation and airway hyperresponsiveness （AHR） were increased in the asthma group. Chrysin significantly inhibited the airway inflammation and AHR, and decreased the levels of IL-4 and IL-13 in BLAF and total IgE levels in serum. In addition, chrysin significantly attenuated the increased protein expression of NF-κB in lung tissues of asthmatic mice. Conclusion： This study demonstrated that chrysin could suppress the progression of airway inflammation and AHR in a murine model of asthma. The effect may be due to inhibition of NF-κB expression.